Pulseless electrical activity overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Maneesha Nandimandalam, M.B.B.S.[2]
Overview
Pulseless electrical activity is defined as the absence of a pulse or cardiac contractility despite the presence of electrocardiographic activity. The most common causes are respiratory failure and hypovolemia, Hypoxia, Hydrogen ions (Acidosis), HypothermiaHyperkalemiaor Hypokalemia, Hypoglycemia, Tablets or Toxins (Drug overdose) such as beta blockers, tricyclic antidepressants, or calcium channel blockers, Tamponade, Tension pneumothorax, Thrombosis (Myocardial infarction), Thrombosis (Pulmonary embolism), Trauma (Hypovolemia from blood loss), Covid-19. PEA is associated with a poor prognosis, particularly if the underlying cause is not readily identifiable and treated. Absence of palpable pulse is the main finding. Echocardiogram can identify several rapidly reversible causes of PEA such as cardiac tamponade, myocardial infarction, cardiac rupture and underfilling of the ventricle due to hypovolemia.
Historical Perspective
Pulseless electrical activity as the main approach for sudden cardiac arrest (SCA) was not completely studied until the middle of the 1980's. The explanation for this, is that ventricular fibrillation (VF) and ventricular tachycardia (VT), were the main causes for the morbidity and mortality of SCA. However there has been a change in approaching the causes of SCA, pointing to PEA as the initial rhythm leading to SCA.
Pathophysiology
PEA( pulseless electrical activity) usually occurs when an insult involves the cardiovascular, gastrointestinal or the respiratory systems. Any such event can lead to decrease in cardiac contractility, and the situation gets even worse by potential acidosis, hypoxia, and worsening vagal tone. A severe initial insult often reduces cardiac output which may in turn cause myocardial ischemia, left ventricular failure, hypoxia and metabolic acidosis. These pathophysiologic disturbances further reduce cardiac output further exacerbating the downward spiral with loss of cardiac output; hypotension, loss of consciousness and apnea rapidly ensue. Other possible mechanisms for pulseless electrical activity include Elevated Afterload, Electromechanical Dissociation, Reduced Contractility, Parasympathetic theory.
Causes
Common causes of PEA include respiratory failure in 40% to 50% of cases, and hypovolemia. Hypovolemia, Hypoxia, Hydrogen ions (Acidosis), HypothermiaHyperkalemiaor Hypokalemia, Hypoglycemia, Tablets or Toxins (Drug overdose) such as beta blockers, tricyclic antidepressants, or calcium channel blockers, Tamponade, Tension pneumothorax, Thrombosis (Myocardial infarction), Thrombosis (Pulmonary embolism), Trauma (Hypovolemia from blood loss), Covid-19.
Risk Factors
The administration of beta blockers and calcium channel blockers is associated with an increased risk of PEA. This may be due to their effect on Ca / troponin interactions, and their inhibition of myocardial contractility.
Natural History, Complications and Prognosis
PEA is associated with a poor prognosis, particularly if the underlying cause is not readily identifiable and treated. The presence of a QRS interval > 0.20 seconds is associated with a poorer prognosis. The survival of in hospital PEA is only 11.2%.[1] The survival for out of hospital occurrence of PEA is higher (19.5%) than for in hospital PEA, likely due to the higher incidence of reversible causes among patients with out of hospital arrest. The survival of PEA as a presenting rhythm is poorer than ventricular tachycardia or ventricular fibrillation.[2]
Diagnosis
Diagnostic Study Of Choice
History and Symptoms
Absence of palpable pulse is the main finding. Depending upon the cause of pulseless electrical activity the following might be found, Tracheal deviation or the unilateral absence of breath sounds in case of tension pneumothorax, decreased skin turgor, Cool extremities, Tachycardia in case of hypotension, traumatic chest, , Cyanosis etc
Echocardiography
A rapid beside echocardiogram can identify several rapidly reversible causes of PEA such as cardiac tamponade, myocardial infarction, cardiac rupture and underfilling of the ventricle due to hypovolemia. Elevated right heart filling pressures suggest pulmonary embolism. Tension pneumothorax can also be observed on a bedside echocardiogram.
Laboratory Findings
Athough there are no diagnostic laboratory findings associated with PEA(pulseless electrical activity) testing should be ordered to rule out the most common reversible causes of PEA(pulseless electrical activity) like Hyperkalemia or Hypokalemia, hypoxia and acidosis which can be seen withABG, exsanguination hematocrit.
Electrocardiogram
The appearance of the electrocardiogram in the setting of PEA varies, but several common patterns exist. There may be a normal sinus rhythm or sinus tachycardia, with discernible P waves and QRS complexes. Sometimes there is a bradycardia, with or without P waves, and often there is a wide QRS complex. The presence of a QRS interval > 0.20 seconds is associated with a poorer prognosis. The EKG should be carefully evaluated for signs of Hyperkalemia, ST segment elevation MI, hypothermia, QRS interval prolongation suggests tricyclic antidepressant overdose
CT scan
There are no CT scan findings associated with pulseless electrical activity. However it can be used to identify some of the causes of pulseless electrical activity like cardiac tamponade, tension pneumothorax.Superior vena cava andInferior vena cava enlargement, Hepatic and renal vein enlargment, Periportal edema, Compression of coronary sinus, Angulation of interventricular septum,Pericardial thickening, Collapse of the right atrium, Aortic blood contrast level these are seen in cardiac tamponade CT.
Treatment
Medical therapy
The current American Heart Association-Advanced Cardiac Life Support (AHA-ACLS) guidelines advise the following be undertaken in all patients start CPR immediately, administer 100% oxygen to reverse hypoxia,Intubate the patient, establish IV access.The mainstay of drug therapy for PEA is epinephrine 1mg every 3–5 minutes.Higher doses of epinephrine can be administered in patients with suspected beta blocker and calcium channel blocker overdose.Immediately after administering epinephrine attention should be directed to reverse any possible causes of PEA as they are the most common causes like hypovolemia (i.e. hypovolemic shock) which should be treated with IV fluidsor packed red blood cell transfusion. Others like electrolyte abnormalities including hyper/hypokalemia should be corrected immediately as they can be life threatening as well as tension pneumothorax.
Surgery
External and internal pacing have not been shown to improve outcome and are not recommended. There may be capture of the signals, but there is no improvement in contractility.
References
- ↑ Nadkarni VM, Larkin GL, Peberdy MA, Carey SM, Kaye W, Mancini ME, Nichol G, Lane-Truitt T, Potts J, Ornato JP, Berg RA (2006). "First documented rhythm and clinical outcome from in-hospital cardiac arrest among children and adults". JAMA : the Journal of the American Medical Association. 295 (1): 50–7. doi:10.1001/jama.295.1.50. PMID 16391216. Retrieved 2012-09-16. Unknown parameter
|month=ignored (help) - ↑ Meaney PA, Nadkarni VM, Kern KB, Indik JH, Halperin HR, Berg RA (2010). "Rhythms and outcomes of adult in-hospital cardiac arrest". Critical Care Medicine. 38 (1): 101–8. doi:10.1097/CCM.0b013e3181b43282. PMID 19770741. Retrieved 2012-09-16. Unknown parameter
|month=ignored (help)